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Fibroblast growth factor 23 modifies the pharmacological effects of angiotensin receptor blockade in experimental renal fibrosis
Author(s) -
Maarten A. de Jong,
Katarina Mirković,
Rik Mencke,
Joost G.J. Hoenderop,
René J.M. Bindels,
Marc G. Vervloet,
JanLuuk Hillebrands,
Jacob van den Born,
Gerjan Navis,
Martin H. de Borst
Publication year - 2016
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfw105
Subject(s) - medicine , losartan , fibrosis , endocrinology , kidney , renin–angiotensin system , angiotensin ii receptor type 1 , mineralocorticoid receptor , kidney disease , angiotensin ii , blockade , pharmacology , receptor , blood pressure
Blockade of the renin-angiotensin-aldosterone system (RAAS) retards progression of chronic kidney disease. Yet, in many patients, the renoprotective effect is incomplete. A high circulating level of the phosphaturic hormone fibroblast growth factor 23 is associated with an impaired response to RAAS blockade-based therapy in clinical studies. Therefore, we addressed whether administration of recombinant fibroblast growth factor 23 (FGF23) interferes with the efficacy of angiotensin receptor blocker (ARB) treatment in a mouse model of renal fibrosis [unilateral ureteral obstruction (UUO)].

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